In aerobic metabolism, the body uses oxygen to produce energy and generates carbon dioxide as a metabolic by-product. The physiological purpose of respiration in this regard is to maintain the proper concentrations of oxygen and carbon dioxide in the blood and other body tissues. As blood flows through the lungs, oxygen from inspired air is absorbed into the blood, while carbon dioxide is removed and blown off during expiration. A principal way in which the rhythm of respiration is regulated is through the respiratory center in the brainstem (in the pons and upper medulla). The respiratory center has chemosensitive areas that respond mainly to the concentration of carbon dioxide in the blood. When blood carbon dioxide increases, the respiratory center sends neural signals to the muscles controlling inspiration and expiration to cause an increase in the depth and/or rate of respiration and vice-versa when blood carbon dioxide decreases.
In certain individuals, a dysfunction in the respiratory control mechanism described above produces a pathological condition known as periodic breathing. One type of periodic breathing, Cheyne-Stokes breathing, is characterized by alternating cycles of hyperventilation and hypoventilation. When hyperventilation occurs, the pulmonary blood becomes excessively depleted of carbon dioxide. After some period of time, the pulmonary blood reaches the respiratory control center in the brain and/or respiratory chemoreceptors in the vasculature to cause suppression of respiration. The resulting hypoventilation then causes carbon dioxide in the pulmonary blood to rise excessively. After a transit time to reach the respiratory control center in the brain, the excessive carbon dioxide in the blood causes hyperventilation that starts the cycle again. In normal individuals, the cycles of hyperventilation and hypoventilation as just described do not occur because the transit time for pulmonary blood to reach the brain is short and the carbon dioxide concentration in the tissues is maintained by the circulation in a manner that buffers increases in the carbon dioxide concentration of pulmonary blood. In certain situations, however, the respiratory control mechanism becomes impaired so that Cheyne-Stokes respiration occurs. In patients with heart failure, cardiac output is decreased below normal and blood flow is correspondingly slow, causing the transit time for pulmonary blood to reach the brain to increase. Cheyne-Stokes respiration frequently occurs in heart failure patients and has been shown to be associated with a poorer prognosis and increased mortality. Abnormally elevated chemoreflex sensitivity associated with increased sympathetic activity is another cause of Cheyne-Stokes respiration, and increased sympathetic activity commonly occurs in heart failure patients. Another cause of Cheyne-Stokes respiration is damage to the respiratory control center in the brain that impairs the feedback mechanism for controlling inspiration and respiration. Damage to the respiratory control center can also cause a related condition known as central sleep apnea in which breathing ceases for prolonged periods during sleep.